This combination of robust DDR checkpoint activation yet rare p53 mutations seems even more counterintuitive given that the activated DDR checkpoints create a pressure for selecting cancer cell clones with mutant p53 as a way to escape the oncogene‐induced, p53‐mediated senescence or cell death of the nascent tumour cells that otherwise often results from the chronic activation of the ATM‐Chk2/ATR‐Chk1‐p53 pathway (Halazonetis et al., 2008). Here, ATM is linked to neoplasm.